Downregulation of TRAP1 aggravates injury of H9c2 cardiomyocytes in a hyperglycemic state.

Abstract

Diabetic cardiomyopathy increases the risk of heart failure and is one of the major causes of death in patients with diabetes. The present study investigated the expression and function of tumor necrosis factor receptor-associated protein 1 (TRAP1) in cardiomyocytes in a hyperglycemic state. For the in vitro study, H9c2 cells (rat cardiomyoblasts) were treated with normal glucose, high glucose. TRAP1 expression was determined by reverse transcription-quantitative PCR and western blot analysis. Viability of cardiomyocytes was detected using the CellTiter 96® AQueous One Solution assay. The intracellular reactive oxygen species (ROS) content was detected using a fluorescent 2',7'-dichlorodihydrofluorescein diacetate probe, and the change in mitochondrial membrane potential was detected by JC-1 fluorescent staining. Changes in cell viability, ROS content and mitochondrial membrane potential were determined following small interfering (si) RNA-mediated knockdown of TRAP1. Results demonstrated that compared with the normal control group, the expression of TRAP1 in H9c2 cells decreased in the high glucose group which was accompanied by a reduction in mitochondrial membrane potential and cell viability, and increased intracellular ROS production. TRAP1 expression was significantly decreased following TRAP1-siRNA transfection which was accompanied by enhanced ROS production, lower mitochondrial membrane potential and impaired cell viability. In conclusion, the present findings suggested that the decrease in cardiomyocyte TRAP1 expression under high glucose conditions was associated with myocardial injury. It was hypothesized that TRAP1 may have a protective role on cardiomyocytes under high glucose surroundings.